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2008-11-22T04:49:00.000-08:00

What Is Acne?
ACNE IS A COMMON skin disease that affects tiny ducts in the skin where hair grows. These ducts are known as follicles. Acne occurs when the follicles become clogged and infected. This causes sores known as acne lesions, or pimples, to develop on and under the skin.
Excess Hormones Cause Excess Oil Production
There are a number of factors that cause the follicles to become clogged and infected. One important factor is the overproduction of androgen. Androgen is a chemical, or male sex hormone, that both males and females normally produce. However, hormonal changes in the body during puberty, pregnancy, or the female menstrual cycle cause some people to produce higher than usual levels of androgen. Although scientists are unsure why, excess androgen stimulates the sebaceous oil glands inside the follicles to enlarge and manufacture excess amounts of oil called sebum. Whereas the normal production of sebum is necessary for healthy skin, excess sebum leads to the development of acne.

Normally, the sebaceous oil glands produce small amounts of sebum, whose job it is to moisten and protect the skin. In order to do this, sebum works its way up through the hair follicles, where it washes away dead cells that accumulate in the follicles. Then sebum empties onto the skin through tiny openings in the follicles called pores. Here sebum protects the skin from bacteria that live on the skin by washing the bacteria away. However, when excess sebum is produced, it accumulates in the follicles rather than spilling out onto the surface of the skin. This occurs because the follicles are extremely small and narrow. Therefore, large volumes of sebum cannot pass through the follicles to the surface of the skin at the rate the sebum is produced. Instead, sebum becomes trapped in the follicles, where it mixes with dead skin cells, forms sticky plugs that block the pores, and prevents sebum from reaching the surface of the skin. As a result, the skin around the clogged follicles dries out. At the same time, since not every follicle becomes clogged, excess oil that spills onto the skin through unclogged follicles causes the skin to feel oily.
What Is Acne?
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Clogged and infected hair follicles like this can cause sores, or acne lesions, to
form under the skin.
Therefore, a person with acne may have dry skin around clogged follicles and oily skin everywhere else.
Worse yet, without sebum to wash away bacteria on the skin, bacteria grow and multiply around the clogged follicles. Eventually, bacteria get inside the clogged follicles, where they mix with sebum and dead cells and cause an infection. This most commonly occurs on the parts of the body that have the largest sebaceous glands, such as the face, chest, neck, shoulders, upper back, and buttocks. The result is the development of one type of acne lesion known as a comedone.

Inflammation Makes Acne Worse
Unfortunately, the damage does not end there. Once bacteria enter the follicles, the immune system, which protects the body from infection and disease, reacts. Blood, rich with infection-fighting white blood cells, rushes to the area. As the infection worsens, pus and other powerful chemicals are also produced to combat the infection. This causes the infected area to become hot, red, swollen, and painful.
Heat, redness, swelling, pain, and the presence of pus are all characteristics of inflammation, which in the case of acne appears on the skin in the form of papules, pustules, and cysts, other types of acne lesions.
Different Types of Lesions
Whether a person develops comedones, papules, pustules, cysts, or a combination of these lesions depends on how severely the hair follicles are clogged and inflamed. The worse the inflammation, the more severe the acne lesion. For example, comedones, which are basically enlarged, clogged hair follicles, form before the hair follicles become inflamed or in the earliest stages of inflammation. Comedones contain sebum, dead skin cells, and bacteria that are trapped in the follicles, but comedones do not contain pus, nor are
they red or swollen. That is why comedones are the least severe type of acne lesion. Since comedones do not contain pus, they are quite small. All comedones have either a white or black tip. Hence, comedones are commonly known as whiteheads or blackheads.

Whiteheads and Blackheads
Whiteheads look like small white bumps and are usually about the size of a pinhead. They form under the skin as the follicles become more and more clogged and enlarged. Whiteheads never reach the skin’s surface or open up. Therefore, they are called closed comedones. Blackheads, on the other hand, are closed comedones that continue to grow upward until they break through the skin’s surface. At this point, the enlarged hair follicle is visible and open to the skin’s surface. For this reason, blackheads are known as open comedones.
To the naked eye the contents of an open comedone look black. The black color is the result of oxidation, a process of discoloration that occurs when dead cells, sebum, and bacteria mix with oxygen in the air. However, some people mistakenly think that dirt trapped.under the skin causes an open comedone to appear black. A young man recalls how this misconception affected him: “I had blackheads all over my forehead and nose. I scrubbed my face constantly, trying to scrub the dirt out of those blackheads. But I kept getting more. I couldn’t understand where all the dirt was coming from.”7 Since comedones do not form as a result of severe inflammation, they are not painful, no matter whether they are blackheads or
whiteheads. Moreover, because comedones are not large, red, or pus filled, when seen from a distance, the skin of people with comedones, especially those with whiteheads, appears relatively clear. However, because comedones are enlarged, clogged follicles, they do not disappear until the follicles unclog. This may not occur under normal circumstances until sebum production decreases or the patient receives effective acne treatment. Therefore, whiteheads and blackheads often stay on or under the skin for a long time. Even more troubling, some closed comedones do not grow upward and become open comedones. Instead, as they become more and more packed with sebum, they grow downward under the surface of the skin and continue to enlarge until they burst. This results in the formation of more serious acne lesions such as papules and pustules.

Papules and Pustules
When closed comedones burst, their contents get into surrounding tissues. In response, the immune system sends more blood to the area, which causes inflammation to begin or worsen. As a result, the closed comedone and the area surrounding it become red and swollen. This redness and swelling appears on the skin in the form of a papule. Papules are small, firm, red bumps. They are only mildly inflamed because they form before pus has reached the area. Therefore, papules are more severe acne lesions than comedones, but milder than acne lesions that contain pus. However, because papules are inflamed, they are often tender to the touch.
As the inflammation worsens, the immune system sends pus tothe area. When this happens, pustules form. Because pustules arecaused by severe inflammation, they often feel hot and may be quite sensitive to the touch.
Not surprisingly, pustules are larger than papules. They are often about the size of the tip of a person’s little finger. Pustules are red at the base, with a yellowish, pus-filled inner region. Aman who had pustules on his face, shoulders, and neck recalls: “They were big old welts filled with white poison and surrounded by red rings.”8
Although a pustule’s red base forms on the surface of the skin, the pus-filled core is near, but still underneath, the skin. However, as inflammation worsens and more pus is formed in the area, the pus-filled core of a pustule begins to swell like a balloon. When this happens, it is not uncommon for pustules to pop open and spill pus onto the skin. Aman recalls: “In the morning before I went to school, I’d have big welts on my shoulders and neck. Sometimes at school they would break without me even knowing. When I got
home I’d have stains on my shirt.”9

Cysts
Just as worsening inflammation causes a pustule to expand upward through the skin’s surface, worsening inflammation also causes pustules to expand downward. When this occurs, a cyst is formed. Cysts are packed with large amounts of pus that extend deep below the skin’s surface. Due to swelling, cysts may be several centimeters in diameter. Most cysts are red or purple and extremely painful. Since cysts form when inflammation and infection are the most severe, cysts are the most serious type of acne lesions.
Three Types of Acne
Just as there are different types of acne lesions, there are also different types of acne. Although there are a number of rare forms of acne, most experts divide acne into three main types: comedonal acne, acne vulgaris, and cystic acne. The first type, comedonal acne, consists of whiteheads and blackheads alone, without the presence of other acne lesions. Therefore, comedonal acne is the mildest form of acne. However, since closed comedones often burst and become inflamed, it is not uncommon for people with comedonal acne eventually to develop papules and pustules.When people have a mix of comedones, papules, and pustules, they have acne vulgaris, or common acne. A man who suffered from acne vulgaris recalls: “I had them all. I had blackheads on my nose. I had whiteheads on my forehead. I had bumpy red pimples and big pus pimples on my chin, neck, back, and shoulders.”10
Acne vulgaris is the most common form of acne, affecting approximately 90 percent of all people with acne. Acne vulgaris can be mild, moderate, or severe, depending on the number of acne lesions a person has and how severely the lesions are inflamed. The third type of acne, cystic acne, is the most severe form of acne. The presence of comedones, papules, pustules, and numerous acne cysts characterize cystic acne. Because cysts are caused by severe inflammation and infection, cystic acne can be quite painful. Making matters worse, if cystic acne is left untreated, the severe inflammation and infection that cause cystic acne can damage surrounding tissues. This frequently leaves the skin of people with cystic acne permanently scarred. Apatient explains: “You can see the scars where I had cysts today. They look like little craters. You can see them on my neck and on my back. I’ve got a little bit of evidence on my face too. Wherever you see a crater, that’s where I had a cyst.”11
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People at Risk
Although almost everyone has an occasional whitehead or blackhead, certain groups are more likely to develop acne vulgaris and cystic acne than others. These include adolescents, adult women, people under stress, people taking certain medications, and people whose parents had acne.

Acne in Adolescents
Adolescents are the largest group at risk of developing acne. This is because acne usually begins during puberty, when the body starts producing androgen. Androgen production is usually at its peak when people are between the ages of twelve and seventeen. Therefore, more oil is produced in the hair follicles of adolescents than in any other age group. As a result, experts estimate that more than 85 percent of all adolescents between the ages of twelve and seventeen develop some form of acne. This translates to more than 20 million teenagers in the United States. Moreover, although both males and females produce androgen, adolescent males produce ten times more androgen than females do because androgen is a male sex hormone. Consequently, it is not surprising that adolescent boys are more likely to develop severe cases of acne vulgaris as well as cystic acne; whereas teenage girls are more likely to develop comedonal acne and mild cases of acne vulgaris.
Generally, oil production decreases after the age of seventeen. In most cases, as androgen and sebum levels decrease, so does acne. Thus, by the time most adolescents reach age eighteen, their acne symptoms begin to subside and disappear. However, approximately 30 percent of all adolescents with acne continue to be plagued with acne for the rest of their lives. According to acne expert and dermatologist Anthony C. Chu, “Acne can persist well into old age and I have a number of patients in their sixties, seventies, and even eighties who still have active acne. Acne is, therefore, not merely a teenage occurrence; it can affect you at any time of your life.”12

Adult Women and Acne
One group that is affected by acne well beyond adolescence is adult women. An estimated 5 percent of adult women have persistent acne that does not subside after puberty. An even larger number develop acne when they reach their twenties or thirties. Many of these women did not have acne as teenagers, while others had acne during their teen years that disappeared when puberty ended. Then, when these women reach their twenties or thirties, acne symptoms reappear as a result of fluctuating hormone levels caused
by pregnancy, their monthly menstrual cycle, or hormonal imbalances. In fact, experts estimate that as many as 50 percent of all adult women suffer from acne. Awoman describes her experience: “I had acne in high school. Luckily, it cleared up my senior year and my face was pretty clear through college. Now I am twentysix, and started getting acne again.”13
Some women experience only occasional acne flare-ups. Since the female menstrual cycle causes hormone levels to rise and fall, many experts believe these flare-ups occur when lower than normal levels of the female sex hormone, estrogen, are being produced. Estrogen is known to counterbalance the production of androgen. Therefore, without sufficient estrogen, androgen production increases unchecked, leading to acne flare-ups. At other times, when estrogen levels are high and androgen levels are low, these women’s skin remains clear. Experts are unsure why this problem does not affect all women, but they theorize it is more likely to occur in women who, for unknown reasons, have the greatest fluctuation in their hormone levels.
Similarly, acne often flares up at different times during pregnancy as a pregnant woman’s hormone levels change in order to accommodate her body’s changing needs. Comparable hormonal changes often occur in some women after they give birth. As a result, some adult women develop acne shortly after their babies are born.

People Under Stress
Stress is another factor that can change hormone levels in adult women, men, and adolescents. Although scientists do not believe that stress directly causes acne, numerous studies have linked stress and acne flare-ups. The reason for this link is that when the body is under stress, it responds by producing hormones, including androgen and cortisol. Cortisol, like androgen, stimulates oil production. Therefore, people who are under stress are at risk of developing acne or having their existing acne worsen. Moreover, even though the production of stress hormones decreases as a person relaxes, stress-induced acne flare-ups often do not clear up until the inflammation heals. This may take a week or more. Chu describes how stress affects his patients: “I have looked after four women who have cancelled their weddings on at least one occasion. Each time they neared their wedding day, stress levels increased and their spots became so bad that they cancelled because they could not bear the thought of wedding photographs of themselves covered with spots.”14

People Taking Medication
Just as stress can change hormone levels, certain medications can also have this effect. For example, although some birth control pills contain estrogen, which lowers androgen levels, one type of birth control pill contains progesterone, a hormone that stimulates the body to produce androgen, which can make acne worse. Other medicines such as those used to treat epilepsy, a disorder that causes seizures, and anabolic steroids, drugs often used illegally by athletes and bodybuilders to stimulate muscle growth, stimulate
the production of androgen and have been linked to acne.

Genetics
Genetics also plays a role in determining who is at risk of developing acne. Experts agree that acne seems to run in families and that there seems to be a direct link between the development of severe acne and familial patterns. Experts are unsure why this is so, since an acne gene has not yet been discovered. However, a number of studies have shown that genetics does play a role in determining how likely a person is to develop acne. Various studies of identical twins, for example, found in over 50 percent of all cases that if one twin develops acne so does the other. Correspondingly, other studies have shown similarities among parents and children regarding the types of acne lesions, the severity of acne, and the duration of acne. Apatient with acne explains: “I inherited it [acne] from my mother, and she’s always telling me that she had the exact same thing and that it will go away. I am mad that I inherited it from her.”15

Physical Effects of Acne
No matter who gets acne, acne can have a long-lasting physical effect. Acne lesions can leave permanent scars on an acne patient’s skin. When a clogged hair follicle becomes infected, and the body sends white blood cells and powerful chemicals to combat the infection, swelling causes tissue around the infected follicle to be damaged. In many cases, once the infection is gone, the tissue is too damaged to return to its normal state. This damage appears in two distinct types of acne scars, scars caused by increased tissue
formation and scars caused by tissue loss. Scars caused by increased tissue formation are called keloid scars. Keloid scars form when the skin responds to tissue injury by producing an excess of collagen, a substance that helps the skin regenerate.Too much collagen causes the production of excess tissue to form over the damaged area. The results are keloid scars, which look like firm, shiny, flesh-colored lumps.
Acne scars that are caused by tissue loss occur when the body is unable to completely rebuild damaged tissue. Often called depressed, ice-pick, or pitted scars, these scars look like the skin has been pushed in, forming a soft depression with puckered edges. Pitted scars can be quite small, or they can be over a centimeter in diameter. Pitted scars are the most common type of acne scar and are commonly found on the face, back, and shoulders. Fortunately, not every person who has acne develops acne scars.
Doctors are unable to predict accurately whether or not a person with acne will develop scars. However, in most cases, as the severity of a person’s acne increases so does the amount of tissue damage. Since acne scars result from damaged tissue, individuals who suffer the most tissue damage are most at risk of developing acne scars. Generally, these are individuals with severe cases of acne.

Emotional Effects of Acne
Even when acne does not cause permanent scars, because acne affects a person’s appearance it can take an emotional toll on a person. People with acne often feel self-conscious about their appearance. Over time, their self-esteem and self-confidence decrease. This makes them feel insecure and anxious in social situations. In fact, many people with acne avoid social situations due to self-consciousness about their appearance. Indeed, many become shy and withdrawn. A young man explains: “I’ve lived with really heavy acne for the last five years. I feel so self-conscious that I don’t even like going out. It’s ruined my confidence.”16
The combination of low self-esteem, embarrassment, and increasing social isolation leads many people with acne to become depressed. When people are depressed, they often lose interest in daily activities and feel tired, anxious, and unhappy. Some may contemplate suicide. In fact, according to a 2002 survey by the Acne Support Group, a British organization that helps acne sufferers, 15 percent of the acne patients surveyed reported feeling suicidal, and 75 percent reported feeling depressed because of acne. An acne patient describes how acne-caused depression affected her: “I did not look in mirrors whatsoever. I walked into a room and immediately shut out the light. Everything I did, I did in darkness because any time I caught a glimpse of myself I felt suicidal.”17
Truly, many people with acne bear both emotional and physical scars all their lives. A former acne patient explains: It’s easy to see the scars on my back and neck. What you can’t see is what it did to me inside. I went from a fairly self-confident kid to an angry, withdrawn, and embarrassed teenager. Even today, the memories of the teasing and the embarrassment are quite vivid. It makes me queasy just to think about it. Even when the pimples are gone, acne stays with you a long time.18

dermatitis

2008-11-21T05:02:00.000-08:00

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Copyright ©2007 The McGraw-Hill Companies. All rights reserved.Fitzpatrick Dermatology Atlas > Part I: Disorders Presenting in the Skin and Mucous Membranes > Section 2. Eczema/Dermatitis >

Eczema/Dermatitis: Introduction
The terms eczema and dermatitis are used interchangeably, denoting a polymorphic inflammatory reaction pattern involving the epidermis and dermis. There are many etiologies and a wide range of clinical findings. Acute eczema/dermatitis is characterized by pruritus, erythema, and vesiculation; chronic eczema/dermatitis, by pruritus, xerosis, lichenification, hyperkeratosis, ± fissuring.

Contact Dermatitis
Contact dermatitis is a generic term applied to acute or chronic inflammatory reactions to substances that come in contact with the skin. Irritant contact dermatitis (ICD) is caused by a chemical irritant; allergic contact dermatitis (ACD) by an antigen (allergen) that elicits a type IV (cell-mediated or delayed) hypersensitivity reaction.
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The acute form of ICD, which in severe cases may even lead to necrosis, occurs after a single exposure to the offending agent that is toxic to the skin (e.g., croton oil, phenols, kerosene, organic solvents, sodium and potassium hydroxide, lime acids). It is dependent on concentration of the offending agent and occurs in everyone, depending on the penetrability and thickness of the stratum corneum. There is a threshold concentration for these substances above which they cause acute dermatitis and below which they do not. This sets acute ICD apart from acute ACD, which is dependent on sensitization and thus occurs only in sensitized individuals. Depending on the degree of sensitization, minute amounts of the offending agents may elicit a reaction. Since ICD is a toxic phenomenon, it is confined to the area of exposure and is therefore always sharply marginated and never spreads. ACD is an immunologic reaction that tends to involve the surrounding skin (spreading phenomenon) and may even spread beyond affected sites. Generalization may occur.

Irritant Contact Dermatitis
ICD is caused by exposure of the skin to chemical or other physical agents that are capable of irritating the skin, acutely or chronically. Severe irritants can cause toxic reactions even after a short exposure. Most cases, however, are caused by chronic cumulative exposure to one or more irritants. The hands are the most commonly affected area. In addition to dermatitis, irritant contact responses of the skin include: subjective irritancy, transient irritant reactions, persistent irritant reactions, toxic (caustic) burn. Irritant contact responses of skin appendages and pigmentary system include: follicular and acneform eruptions, miliaria, pigmentary changes (hypo- and hyperpigmentation), granulomatous reactions, and alopecia.
Epidemiology
ICD is the most common form of occupational skin disease, accounting for up to 80% of all occupational skin disorders. However, ICD need not be occupational and can occur in anyone being exposed to a substance irritant or toxic to the skin.
Occupational Exposure
Individuals engaged in the following occupations/activities are at risk for ICD: housekeeping; hairdressing; medical, dental, and veterinary services; cleaning; floral arranging; agriculture; horticulture; forestry; food preparation and catering; printing; painting; metal work; mechanical engineering; car maintenance; construction; fishing.
Etiology
Etiologic Agents
(Table 2-1) Abrasives, cleaning agents, oxidizing agents (e.g., sodium hypochlorite); reducing agents (e.g., phenols, hydrazine, aldehydes, thiophosphates), plants (e.g., spurge, Boracinaceae, Ranunculaceae), animal enzymes, secretions; dessicant powders, dust, soils; excessive exposure to water.
Table 2-1 Most Common Irritant/Toxic Agents
Soaps, detergents, waterless hand cleaners
Acids and alkalis*: hydrofluoric acid, cement, chromic acid, phosphorus, ethylene oxide, phenol, metal salts.
Industrial solvents: coal tar solvents, petroleum, chlorinated hydrocarbons, alcohol solvents, ethylene glycol ether, turpentine, ethyl ether, acetone, carbon dioxide, DMSO, dioxane, styrene.
Plants: Euphorbiaceae (spurges, crotons, poinsettias, machneel tree). Racunculaceae (buttercup), Cruciferae (black mustard), Urticaceae (nettles), Solanaceae (pepper, capsaicin), Opuntia (prickly pear).
Others: fiberglass, wool, rough synthetic clothing, fire-retardant fabrics, "NCR" paper.

* Lead to chemical burns and necrosis, if concentrated.
Predisposing Factors
Atopics with a history of atopic dermatitis are at highest risk for ICD; the majority of workers with significant occupational ICD are atopics. Others: white skin, temperature (low), climate (low humidity), occlusion, mechanical irritation. Cement ICD tends to flare in summer in hot humid climates.
Pathogenesis
Both chemical and physical agents can be irritants, causing cell damage if applied for sufficient time and in adequate concentration. ICD occurs when defense or repair capacity of the skin is unable to maintain normal skin integrity and function or when penetration of chemical(s) induces an inflammatory response. Lesser irritants cause reaction only after prolonged exposure. The initial reaction is usually limited to the site of contact with the irritant; the concentration of irritant diffusing outside the area of contact almost always falls below the critical threshold necessary to provoke a reaction.
Mechanisms involved in acute and chronic phases of ICD are fundamentally different. Acute reactions involve direct cytotoxic damage to keratinocytes. Chronic ICD results from repeated exposures to solvents and surfactants that cause slow damage to cell membranes, disrupting the skin barrier and leading to protein denaturation and cellular toxicity.
Acute Irritant Contact Dermatitis
Symptoms
In some individuals, subjective symptoms (burning, stinging, smarting) may be the only manifestations. Painful sensations can occur within seconds after exposure (immediate-type stinging), e.g., to acids, chloroform, and methanol. Delayed-type stinging occurs within 1 to 2 min, peaking at 5 to 10 min, fading by 30 min, and is caused by agents such as aluminum chloride, phenol, propylene glycol, and others. In acute delayed ICD, objective skin symptoms do not start until 8 to 24 after exposure (e.g., anthralin, ethylene oxide, benzalconium chloride) and are accompanied by burning rather then itching.
Physical Examination
Skin Findings
May occur minutes after exposure or may be delayed up to 24 h. The spectrum of changes ranges from erythema to vesiculation (Figs. 2-1 and 2-2) and caustic burn with necrosis. Acute ICD represents sharply demarcated erythema and superficial edema, corresponding to the application site of the toxic substance (Fig. 2-1). Lesions do not spread beyond the site of contact. In more severe reactions vesicles and blisters arise within the erythematous lesions (Fig. 2-2), followed by erosions and/or even frank necrosis, as with acids or alkline solutions. No papules. Configuration often bizarre or linear ("outside job" or dripping effect).
Evolution of Lesions
Erythema with a dull, nonglistening surface (Fig. 2-1) vesiculation (or blister formation) (Fig. 2-2) erosion crusting shedding of crusts and scaling or (in chemical burn) erythema necrosis shedding of necrotic tissue ulceration healing.

Distribution
Isolated, localized to one region or generalized (plant dermatitis), depending on contact with toxic agent.

Duration
Days, weeks depending on tissue damage.
Constitutional Symptoms
Usually none, but in widespread acute ICD "acute illness" syndrome, including fever.
Chronic Irritant Contact Dermatitis
Types
Cumulative ICD
Most common; develops slowly after repeated additive exposure to mild irritants (water, soap, detergents etc.), usually on hands. Repeated exposures to toxic or subtoxic concentrations of offending agents usually associated with a chronic disturbance of the barrier function that allows even subtoxic concentrations of offending agents to penetrate into the skin and elicit a chronic inflammatory response; e.g., after repeated exposure to alkaline detergents and organic solvents, which, if applied only once to normal skin, do not elicit a reaction. Injury (e.g., repeated rubbing of the skin), prolonged soaking in water, or chronic contact after repeated, cumulative physical trauma — friction, pressure, abrasions in individuals engaged in manual work (traumatic ICD).
Irritant Reaction ICD
Early, subclinical dermatitis on hands of individuals exposed to wet work. Usually during first months of training of hair dressers or of metal workers.
Symptoms
Stinging and itching, pain as fissures develop.
Physical Examination
Skin Findings
Dryness chapping erythema hyperkeratosis and scaling fissures and crusting (Fig. 2-3). Sharp margination gives way to ill-defined borders, lichenification. In irritant reaction ICD also vesicles, pustules, and erosions.
Distribution
Usually on hands (Fig. 2-3). In cumulative ICD usually starting at finger web spaces, spreading to sides and dorsal surface of hands and then to palms. In housewives often starting on finger tips (pulpitis). Rarely in other locations exposed to irritants and/or trauma, e.g., in violinists on mandible or neck, or on exposed sites as in airborne ICD (see below).
Duration
Chronic, months to years.
Constitutional Symptoms
None, except when infection occurs. Chronic ICD (e.g., hand dermatitis; see below) can become a severe occupational and emotional problem.
Laboratory Examination
Histopathology
In acute ICD, epidermal cell necrosis, neutrophils, vesiculation, and necrosis. In chronic ICD, acanthosis, hyperkeratosis, lymphocytic infiltrate.
Patch Tests
These are negative in ICD unless allergic contact dermatitis is also present (see below).
Special Forms of ICD
Hand Dermatitis
Most cases of chronic ICD occur on the hands and are occupational. Often sensitization to allergens (such as nickel or chromate salts) occurs, and then ACD (acute and/or chronic) is superimposed on ICD. A typical example is hand dermatitis in construction and cement workers. Cement is alkaline and corrosive, leading to chronic ICD; chromates in cement sensitize and lead to ACD. In such cases the eruption may spread beyond the hands and may even generalize.
Airborne ICD
Characteristically face, neck, anterior chest, and arms are involved. Most frequent causes are irritating dust and volatile chemicals (ammonia, solvents, formaldehyde, epoxy resins, cement, fiberglass, sawdust from toxic woods). This has to be distinguished from photoallergic contact dermatitis (see Photoallergic Drug-/Chemical-Induced Photosensitivity).
Pustular and Acneiform ICD
ICD may target follicles and become pustular and papulopustular. It may result from metals, mineral oils, greases, cutting fluids, naphthalenes.
Diagnosis and Differential Diagnosis
Diagnosis is by history and clinical examination (lesions, pattern, site). Most important differential diagnosis is ACD (see Table 2-3). On palms and soles: palmoplantar psoriasis; in exposed sites: photoallergic contact dermatitis.
Table 2-3 Differences Between Irritant and Allergic Contact Dermatitis*

Irritant CD
Allergic CD
Symptoms
Acute
Stinging, smarting ⇛ itching
Itching ⇛ pain

Chronic
Itching/pain
Itching/pain
Lesions
Acute
Erythema ⇛ vesicle ⇛ erosion ⇛ crust ⇛ scaling
Erythema ⇛ papules ⇛ vesicles ⇛ erosions ⇛ crust ⇛ scaling

Chronic
Papules, plaques, fissures, scaling, crusts
Papules, plaques, scaling, crusts
Margination and site
Acute
Sharp, strictly confined to site of exposure
Sharp, confined to site of exposure but spreading in the periphery; usually tiny papules; may become generalized

Chronic
Ill-defined
Ill-defined, spreads
Evolution
Acute
Rapid (few hours after exposure)
Not so rapid (12 to 72 h after exposure)

Chronic
Months to years of repeated exposure
Months or longer; exacerbation after every reexposure
Causative agents

Dependent on concentration of agent and state of skin barrier; occurs only above threshold level
Relatively independent of amount applied, usually very low concentrations sufficient but depends on degree of sensitization
Incidence

May occur in practically everyone
Occurs only in the sensitized

* Differences are printed in bold.
Course and Prognosis
Healing usually occurs within 2 weeks of removal of noxious stimuli; in more chronic cases, 6 weeks or longer may be required. In the setting of occupational ICD, only one-third of individuals have complete remission and may require allocation to another job; atopic individuals have a worse prognosis. In cases of chronic subcritical levels or irritant, some workers develop tolerance or "hardening."
Management
Prevention
Prevention: Introduction
Avoid irritant or caustic chemical(s) by wearing protective clothing (i.e., goggles, shields, gloves).
If contact does occur, wash with water or weak neutralizing solution.
Barrier creams.
In occupational ICD that persists in spite of adherence to the above measures, change of job may be necessary.
Treatment
Acute
Identify and remove the etiologic agent. Wet dressings with gauze soaked in Burow's solution, changed every 2 to 3 h. Larger vesicles may be drained, but tops should not be removed. Topical class I glucocorticoid preparations. In severe cases, systemic glucocorticoids may be indicated. Prednisone: 2-week course, 60 mg initially, tapering by steps of 10 mg.
Subacute and Chronic
Identify and remove etiologic/pathogenic agent. Employ a potent topical glucocorticoid preparation, betamethasone dipropionate or clobetasol propionate, and provide adequate lubrication. As healing occurs, continue with lubricating/protective creams or ointments.
In chronic ICD of hands a "hardening effect" can be achieved in most cases with topical (soak or bath)-PUVA therapy (see Palms and Soles). The newer topical anti-inflammatory agents (pimecrolimus and tacrolimus) are being evaluated.

Allergic Contact Dermatitis

One of the most frequent, vexing, and costly skin problems. An eczematous (papules, vesicles, pruritic) dermatitis due to reexposure to a substance to which the individual is sensitized.
Epidemiology
Frequent. Accounts for 7% of occupationally related illnesses in the United States. However, there are data suggesting that the actual indicence rate is 10 to 50 times greater than reported in the U.S. Bureau of Labor Statistics data. In addition, nonoccupational ACD is estimated to be three times greater than occupational ACD.
Age of Onset
No influence on capacity for sensitization; however, allergic contact dermatitis is uncommon in young children and in individuals older than 70 years.
Occupation
One of the most important causes of disability in industry.
Pathogenesis
ACD is a classic, delayed, cell-mediated hypersensitivity reaction. Exposure to a strong sensitizer such as poison ivy resin results in sensitization in a week or so, while exposure to a weak allergen may take months to years for sensitization. The antigen is taken up by Langerhans cells in the epidermis, which process the antigen and migrate from the epidermis to the draining lymph nodes, where they present the processed antigen in association with MHC class II molecules to T cells that then proliferate. Sensitized T cells leave the lymph node, enter the blood circulation, home to the skin, and, after being presented by Langerhans cells with the same specific antigen, produce and mediate the release by other cells of a variety of cytokines. Thus, all the skin becomes hypersensitive to the contact allergen and will react wherever the specific allergen is represented.
Allergens
Contact allergens are diverse and range from metal salts to antibiotics, dyes to plant products. Thus, allergens are found in jewelry, personal care products, topical medications, plants, house remedies, and chemicals the individual may come in contact with at work. The most common allergens in the United States are listed in Table 2-2.
Table 2-2 Top Ten Contact Allergens (North American Contact Dermatitis Group) and Other Common Contact Allergens
Allergen
Principal Sources of Contact
Nickel sulfate
Metals, metals in clothing, jewelry, catalyzing agents
Neomycin sulfate
Usually contained in creams, ointments
Balsam of Peru
Topical medications
Fragrance mix
Fragrances, cosmetics
Thimerosal
Antiseptics
Sodium gold thiosulfate
Medication
Formaldehyde
Disinfectant, curing agents, plastics
Quaternium-15
Disinfectant
Cobalt chloride
Cement, galvanization, industrial oils, cooling agents, eyeshades
Bacitracin
Ointments, powder

Methyldibromoglutaronitrile, phenoxylethanol
Preservatives, cosmetics
Carba mix
Rubber, latex
Ethyleneurea melamine-formaldehyde resin
Textile additives
Thiuram
Rubber
p-Phenylene diamine
Black or dark dyes of textiles, printer's ink
Parahydroxybenzoic acid ester
Conserving agent in foodstuffs
Propylene glycol
Preservatives, cosmetics
Procaine, benzocaine
Local anesthetics
Sulfonamides
Medication
Turpentine
Solvents, shoe polish, printer's ink
Mercury salts
Disinfectant, impregnation
Chromates
Cement, antioxidants, industrial oils, matches, leather
Cinnamic aldehyde
Fragrance, perfume
History
The eruption starts in a sensitized individual 48 h or days after contact with the allergen; repeated exposures lead to a crescendo reaction, i.e., the eruption worsens. Site of the eruption is confined to site of exposure.
Symptoms
Subjective symptoms are intense pruritus; in severe reactions also stinging and pain.
Constitutional Symptoms
"Acute illness" syndrome, including fever, but only in severe allergic contact dermatitis (e.g., poison ivy).
Physical Examination
Skin Lesions
The appearance of ACD depends on severity, location, and duration.
Type
Acute
Well-demarcated erythema and edema on which are superimposed closely spaced, nonumbilicated vesicles, and/or papules (Figs. 2-4 and 2-5); in severe reactions, bullae, confluent erosions exuding serum, and crusts (Fig. 2-6).
Subacute
Plaques of mild erythema showing small, dry scales, sometimes associated with small, red, pointed or rounded, firm papules.
Chronic
Plaques of lichenification (thickening of the epidermis with deepening of the skin lines in parallel or rhomboidal pattern), scaling with satellite, small, firm, rounded or flat-topped papules, excoriations, erythema, and pigmentation.
Arrangement
Initially, confined to area of contact with allergen [e.g., earlobe (earrings), dorsum of foot (shoes), wrist (watch or watch-band), collar-like (necklace), lips (lipstick)]. Often linear, with artificial patterns, an "outside job." Plant contact often results in linear lesions (e.g., Rhus dermatitis). Initially confined to site of contact, later spreading beyond.
Distribution
Extent
Isolated, localized to one region (e.g., shoe dermatitis), or generalized (e.g., plant dermatitis).
Pattern
Random or on exposed areas (as in airborne ACD).
Course
Evolution of ACD
The duration of ACD varies among individuals, resolving in some in 1 to 2 weeks. ACD continues to get worse as long as allergen continues to come into contact with the skin.
Acute
Erythema papules vesicles erosions crusts scaling.
Note: In the acute forms of contact dermatitis, papules occur only in ACD, not in ICD.
Chronic
Papules scaling lichenification excoriations. Chronic inflammation with thickening, fissuring, scaling, and crusting results.
Note: Contact dermatitis is always confined to the site of exposure to the allergen. Margination is originally sharp in ACD; however, it spreads in the periphery beyond the actual site of exposure. If strong sensitization has occurred, spreading to other parts of the body and generalization occur. The main differences between toxic irritant and allergic contact dermatitis are summarized in Table 2-3.
Laboratory Examinations
Dermatopathology
Acute
Prototype of spongiotic dermatitis. Inflammation with intraepidermal intercellular edema (spongiosis), lymphocytes and eosinophils in the epidermis, and monocyte and histiocyte infiltration in the dermis.
Chronic
In chronic ACD there are also spongiosis plus acanthosis, elongation of rete ridges, and elongation and broadening of papillae; hyperkeratosis; and a lymphocytic infiltrate.
Patch Tests
In ACD sensitization is present on every part of the skin; therefore, application of the allergen to any area of normal skin provokes an eczematous reaction. A positive patch test shows erythema and papules, as well as possibly vesicles confined to the test site. Patch tests should be delayed until the dermatitis has subsided for at least 2 weeks and should be performed on a previously uninvolved site. (See Clinical Tests.)
Diagnosis and Differential Diagnosis
By history and clinical findings including evaluation of site and distribution. Histopathology may be helpful; verification of offending agent (allergen) by patch test. Exclude ICD (Table 2-3), atopic dermatitis, seborrheic dermatitis (face), psoriasis (palms and soles), epidermal dermatophytosis (KOH), fixed drug eruption, erysipelas phytophotodermatitis.
Special Forms of ACD
Allergic Contact Dermatitis Due to Plants
Allergic contact dermatitis associated with plants, termed allergic phytodermatitis (APD), occurs in sensitized individuals after exposure to a wide variety of plant allergens and is characterized by an acute, very pruritic, eczematous dermatitis, often in a linear arrangement. In the United States, poison ivy/oak are by far the most common plants implicated. In contrast, phytophotodermatitis is a photosensitivity reaction occurring in any individual with a photosensitizing plant-derived chemical on the skin and subsequent sun exposure (see Section 10).
Synonyms: Poison oak dermatitis, poison ivy dermatitis, toxicodendron dermatitis.
Epidemiology and Etiology
Age of Onset
Occurs in individuals of all ages. Very young and very old are less likely to be sensitized to plants. Sensitization is lifelong.
Etiology
Pentadecylcatechols, present in the Anacardiaceae plant family, are the most common sensitizers in the United States. Pentadecylcatechols cross-react with other phenolic compounds such as resorcinol, hexylresorcinol, and hydroxyquinones.
Plants
Anacardiaceae Family
Poison ivy (Toxicodendron radicans) and poison oak (T. querifolium, T. diversilobum). Also poison sumac (T. vernix). Plants related to poison ivy group: Brazilian pepper, cashew nut tree, ginkgo tree, Indian marker nut tree, lacquer tree, mango tree, rengas tree.
Geography
Poison ivy occurs throughout the United States (except extreme southwest) and southern Canada; poison oak on the west coast. Poison sumac and poison dogwood grow only in woody, swampy areas.
Exposure
Telephone and electrical workers working outdoors. Leaves, stems, seeds, flowers, berries, and roots contain milky sap that turns to a black resin on exposure to air. Cashew oil: unroasted cashew nuts (heat destroys hapten); cashew oil in wood (Haitian voodoo dolls, swizzle sticks), resins, printer's ink. Mango rind. Marking nut tree of India: laundry marker (dhobi itch). Furniture lacquer from Japanese lacquer tree.
Season
APD usually occurs in the spring, summer, and fall; can occur year-round if exposed to stems or roots. In southwest of the United States, occurs year-round.
Pathogenesis
All Toxicodendron plants contain identical allergens. Hapten is present in milky sap in leaves, stems, seeds, flowers, berries, and roots. The oleoresins are referred to as urushiol. The haptens are the pentadecylcatechols (1,2-hydroxybenzenes with a 15-carbon side chain in position three). Washing with soap and water removes oleoresins.
More than 70% of individuals can be sensitized to Toxicodendron haptens. Dark-skinned individuals are less susceptible to APD. After first exposure (sensitization) dermatitis occurs 7 to 12 days later. In a previously sensitized person (may be many decades before), dermatitis occurs (especially on face or genitalia) in <12 h after reexposure. Difference in clinical course varies with individual reactivity, inoculum of hapten on skin, and regional variation.
Note: Blister fluid does not contain hapten and cannot spread the dermatitis; exposure to smoke from the burning plant is harmless, but dermatitis can occur from particulate matter in the smoke.
History
Exposure
Poison Ivy/Oak Dermatitis
Direct plant exposure: plant brushes against exposed skin giving rise to linear lesions (Fig. 2-7); resin usually is not able to penetrate the thick stratum corneum of palms/soles. Clothing: wearing clothing previously contaminated with resin can reexpose the skin.
Food Containing Urushiol
Eating unpeeled mango or unroasted cashew nuts can expose lips to oleoresin. Mucous membranes uncommonly experience APD but ingestion of urushiol can produce allergic contact dermatitis of the anus and perineum.
Skin Symptoms
Pruritus mild to severe. Often sensed before any detectable skin changes. Pain in some cases. Secondary infection associated with local tenderness.
Constitutional Symptoms
Sleep deprivation due to pruritus.
Physical Examination
Skin Lesions
Initially, well-demarcated patches of erythema, characteristic linear lesions (Fig. 2-7); rapidly evolve into papules and edematous plaques; may be severe especially on face and/or genitals, resembling cellulitis (Fig. 2-8). Microvesiculation may evolve to vesicles and/or bullae. Erosions, crusts. With resolution, erythematous plaques ±scale, ±erosion, ±crusting. Postinflammatory hyperpigmentation common in darker skinned individuals.
Distribution
Most commonly on exposed extremities, where contact with the plant occurs; blotting can transfer to any exposed site; palms/soles are usually spared; however, lateral fingers can be involved.
Clothing-Protected Sites
Oleoresin can penetrate damp clothing onto covered skin.
Nonexposed Sites
"Id"-like reaction or some systemic absorption can be associated with disseminated urticarial, erythema multiforme-like, or scarlatiniform lesions away from sites of exposure in some individuals with well-established APD.
Laboratory Examinations
Dermatopathology
See ACD, above.
Patch Tests with Pentadecylcatechols
Contraindicated. Can sensitize the individual to hapten.
Diagnosis
By history and clinical findings.
Differential Diagnosis
ACD to other allergens, phytophotodermatitis, soft-tissue infection (cellulitis, erysipelas), atopic dermatitis, inflammatory dermatophytosis, early herpes zoster, fixed drug eruption.
Systemic ACD (SACD)
After systemic exposure to an allergen to which the individual had prior ACD. A delayed T cell–mediated reaction. Examples: ACD to ethylenediamine subsequent reaction to aminophylline (which contains ethylene diamine); poison ivy dermatitis subsequent reaction to ingestion of cashew nuts; also antibiotics, sulfonamides, propylene glycol, metal ions, sorbic acid, fragrances.
Airborne ACD
Contact with airborne allergens in exposed body sites, notably the face (Fig. 2-9); also including eyelids, "V" of the neck, arms, and legs. In contrast to airborne ICD, papular from the beginning, extremely itchy. Prolonged repetitive exposure leads to dry, lichenified ACD with erosions and crusting (Fig. 2-9). Due to plant allergens, especially from compositae, natural resins, woods, essential oils volatizing from aroma therapy.
Management of ACD
Termination of Exposure
Identify and remove the etiologic agent.
Topical Therapy
Topical glucocorticoid ointments/gels (classes I to III) are effective for early nonbullous lesions. Larger vesicles may be drained, but tops should not be removed. Wet dressings with cloths soaked in Burow's solution changed every 2 to 3 h. Since treatment with glucocorticoids is usually short-term in ACD, there is usually no danger of glucocorticoid side effects. An exception is airborne ACD, which may require systemic treatment. The newer immunomodulating topicals pimecrolimus and tacrolimus are effective in ACD but are still being evaluated.
Systemic Therapy
Glucocorticoids are indicated if severe (i.e., if patient cannot perform usual daily functions, cannot sleep) for exudative lesions. Prednisone beginning at 70 mg (adults), tapering by 5 to 10 mg/d over a 1- to 2-week period.
In airborne ACD where complete avoidance of allergen may be impossible, immunosuppression with oral cyclosporine may become necessary.

Atopic Dermatitis

Atopic dermatitis (AD) is an acute, subacute, or chronic relapsing skin disorder that usually begins in infancy and is characterized principally by dry skin and pruritus; consequent rubbing and scratching lead to lichenification and hence to further itching and scratching (itch-scratch cycle). The diagnosis is based on clinical findings, although the serum IgE level is usually (85%) elevated. AD is often associated with a personal or family history of AD, allergic rhinitis, and asthma; 35% of infants with AD develop asthma later in life.
Synonyms: IgE dermatitis, "eczema," atopic eczema.
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Epidemiology
Age of Onset
First 2 months of life and by the first years in 60% of patients. 30% are seen for the first time by age 5, and only 10% develop AD between 6 and 20 years of age. Rarely AD has an adult onset.
Gender
Slightly more common in males than females.
Prevalence
Between 7 and 15% reported in population studies in Scandinavia and Germany.
Genetic Aspects
The inheritance pattern has not been ascertained. However, in one series, 60% of adults with AD had children with AD. The prevalence in children was higher (81%) when both parents had AD.
Eliciting Factors
Inhalants
Specific aeroallergens, especially dust mites and pollens, have been shown to cause exacerbations of AD.
Microbial Agents
Exotoxins of Staphylococcus aureus may act as superantigens and stimulate activation of T cells and macrophages.
Autoallergens
Sera of patients with AD contain IgE antibodies directed at human proteins. The release of these autoallergens from damaged tissue could trigger IgE or T cell responses, suggesting maintenance of allergic inflammation by endogenous antigens.
Foods
Subset of infants and children have flares of AD with eggs, milk, peanuts, soybeans, fish, and wheat.
Other Exacerbating Factors
Skin Barrier Disruption:
decrease of barrier function associated with reduced ceramide levels and increased transepidermal water loss by frequent bathing and hand washing; dehydration is an important exacerbating factor.
Infections:
S. aureus is almost always present in severe cases; group A streptococcus; rarely fungus (dermatophytosis, candidiasis).
Season:
in temperate climates, AD usually improves in summer, flares in winter.
Clothing:
pruritus flares after taking off clothing. Wool is an important trigger; wool clothing or blankets directly in contact with skin (also wool clothing of parents, fur of pets, carpets).
Emotional Stress:
results from the disease or is itself an exacerbating factor in flares of the disease.
Pathogenesis
Complex interaction of skin barrier, genetic, environmental, pharmacologic, and immunologic factors. Type I (IgE-mediated) hypersensitivity reaction occurring as a result of the release of vasoactive substances from both mast cells and basophils that have been sensitized by the interaction of the antigen with IgE (reaginic or skin-sensitizing antibody). The role of IgE in AD is still not fully clarified, but epidermal Langerhans cells possess high-affinity IgE receptors through which an eczema-like reaction can be mediated. TH2 and TH1 both contribute to skin inflammation in AD. Actute T cell infiltration in AD is associated with a predominance of interleukin (IL) 4 and IL-13 expression, and chronic inflammation in AD with increased IL-5, granulocyte-macrophage colony-stimulating factor (GM-CSF), IL-12, and interferon (IFN) . Thus, skin inflammation in AD shows a biphasic pattern of T cell activation.
History
Skin Symptoms
Patients have dry skin. Pruritus is the sine qua non of atopic dermatitis—"eczema is the itch that rashes." The constant scratching leads to a vicious cycle of itch scratch rash itch.
Other Symptoms of Atopy
Allergic rhinitis, characterized by sneezing, rhinorrhea, obstruction of nasal passages, conjuctival and pharyngeal itching, and lacrimation; may be seasonal when associated with pollen.
Physical Examination
Skin Lesions
Acute
Poorly defined erythematous patches, papules, and plaques with or without scale. Edema with widespread involvement; skin appears "puffy" and edematous (Fig. 2-10). Erosions: moist, crusted. Linear or punctate, resulting from scratching. Secondarily infected sites: S. aureus. Oozing erosions (Figs. 2-11 and 2-12) and/or pustules (usually follicular). Crusts.
Chronic
Lichenification (thickening of the skin with accentuation of skin markings): results from repeated rubbing or scratching (Fig. 2-13); follicular lichenification (especially in brown and black persons) (Fig. 2-14). Fissures: painful, especially in flexures (Fig. 2-15), on palms, fingers, and soles. Alopecia: lateral one-third of the eyebrows as a result of rubbing. Periorbital pigmentation: also as a result of compulsively rubbing. Characteristic infraorbital fold in the eyelids (Dennie-Morgan sign).
Distribution
Predilection for the flexures, front and sides of the neck, eyelids, forehead, face, wrists, and dorsa of the feet and hands (Image 2-1). Generalized in severe disease.
Special Features Related to Ethnicity
In blacks, so-called follicular eczema is common and is characterized by discrete follicular papules (Fig. 2-14) involving all hair follicles of the involved site.
Special Features Related to Age
Infantile AD
The lesions present as red skin, tiny vesicles on "puffy" surface. Scaling, exudation with wet crusts and cracks (fissures) (Figs. 2-10, 2-11, and 2-12). Skin lesions seem to be a reaction to itching and rubbing.
Childhood-Type AD
The lesions are papular, lichenified plaques, erosions, crusts, especially on the antecubital and popliteal fossae (Figs. 2-13, 2-14, 2-15, and 2-16), the neck and face.
Adult-Type AD
There is a similar distribution, with lichenification and exoriations being the most conspicuous symptoms (Fig. 2-17).
Associated Findings
"White" dermatographism is a special and unique feature of involved skin: stroking will not lead to redness as in normal skin but to blanching; delayed blanch to cholinergic agents. Ichthyosis vulgaris and keratosis pilaris occur in 10% of patients. Vernal conjuctivitis with papillary hypertrophy or cobblestoning of upper eyelid conjuctiva. Atopic keratoconjunctivitis is disabling, may result in corneal scarring. Keratoconus rare. Cataracts in a small percentage.
Diagnosis
History in infancy, clinical findings (typical distribution sites, morphology of lesions, white dermatographism).
Differential Diagnosis
Seborrheic dermatitis, ICD, ACD, psoriasis, nummular eczema, dermatophytosis, early stages of mycosis fungoides. Rarely, acrodermatitis enteropathica, glucagonoma syndrome, histidinemia, phenylketonuria; also, some immunologic disorders including Wiskott-Aldrich syndrome, X-linked agammaglobulinemia, hyper-IgE syndrome, Letterer-Siwe disease, and selective IgA deficiency.
Laboratory Examinations
Bacterial Culture
Colonization with S. aureus is very common in the nares and in the involved skin; almost 90% of patients with severe AD are secondarily colonized/infected. Look out for MRSA.
Viral Culture
Rule out herpes simplex virus (HSV) infection in crusted lesions (eczema herpeticum; see Section 25).
Blood Studies
Increased IgE in serum, eosinophilia.
Dermatopathology
Various degrees of acanthosis with rare intraepidermal intercellular edema (spongiosis). The dermal infiltrate is composed of lymphocytes, monocytes, and mast cells with few or no eosinophils.
Special Forms of AD
Hand Dermatitis
Aggravated by wetting and washing with detergents, harsh soaps, and disinfectants; leads to ICD in the atopic. Clinically indistinguishable from "normal ICD" (see Special Forms of ICD).
Exfoliative Dermatitis
(See Section 8) Erythroderma in patients with extensive skin involvement. Generalized redness, scaling, weeping, crusting, lymphadenopathy, fever, and systemic toxicity.
Course and Prognosis
Untreated involved sites persist for months or years. Spontaneous, more or less complete remission during childhood occurs in >40% with occasional, more severe recurrences during adolescence. In many patients, the disease persists for 15 to 20 years, but is less severe. From 30 to 50% of patients develop asthma and/or hay fever. Adult-onset AD often runs a severe course. S. aureus infection leads to extensive erosions and crusting, and herpes simplex infection to eczema herpeticum, which may be life-threatening (see Section 25).
Management
Education of the patient to avoid rubbing and scratching is most important. Topical antipruritic (menthol/camphor) lotions are helpful in controlling the pruritus but are useless if emollients are not used and the patient continues to scratch and rub the plaques.
An allergic workup is rarely helpful in uncovering an allergen; however, in patients who are hypersensitive to house dust, mites, various pollens, and animal hair proteins, exposure to the appropriate allergen may cause flares. Atopic dermatitis is considered by many to be related, at least in part, to emotional stress.
Patients should be warned of their special problems with herpes simplex and the frequency of superimposed staphylococcal infection, for which oral antibiotics are indicated. Antiviral drugs for herpes simplex are indicated if HSV infection is suspected.
Acute
1. Wet dressings and topical glucocorticoids; topical antibiotics (mupirocin ointment) when indicated.
2. Hydroxyzine, 10 to 100 mg qid for pruritus.
3. Oral antibiotics (dicloxacillin, erythromycin) to eliminate S. aureus and treat MRSA according to sensitivity as shown by culture.
Subacute and Chronic
1. Hydration (oilated baths or baths with oatmeal powder) followed by application of unscented emollients (e.g., hydrated petrolatum) form the basic daily treatment needed to prevent xerosis. Soap showers are permissible to wash the body folds, but soap should seldom be used on the other parts of the skin surface. 12% ammonium lactate or 10% -hydroxy acid lotion is very effective for the xerosis seen in AD.
2. Topical anti-inflammatory agents such as glucocorticoids, hydroxyquinoline preparations, and tar are the mainstays of treatment. Of these, glucocorticoids are the most effective. However, topical glucocorticoids may lead to skin atrophy if used for prolonged periods of time and if used excessively will lead to suppression of the pituitary-adrenal axis, osteoporosis, growth retardation. Another problem is "glucocorticoidophobia." Patients or their parents are increasingly aware of glucocorticoid side effects and refuse their use, no matter how beneficial they may be.
3. New nonsteroidal anti-inflammatory agents are now available and will probably replace glucocorticoids for most patients in the future. These are topical tacrolimus and pimecrolimus. They potently suppress itching and inflammation and do not lead to skin atrophy. The only problem with tacrolimus is that some patients cannot tolerate the immediate (but transient) burning on application. Burning is less of a problem with pimecrolimus.
4. Oral H1 antihistamines are useful in reducing itching.
5. Systemic glucocorticoids should be avoided, except in rare instances in adults for only short courses (rescue treatment). They are widely overused. Osteopenia and cataracts are complications. For severe intractable disease, prednisone, 60 to 80 mg daily for 2 days, then halving the dose each 2 days for the next 6 days. Patients with AD tend to become dependent on oral glucocorticoids. Often, small doses (5 to 10 mg) make the difference in control and can be reduced gradually to even 2.5 mg/d, as is often used for the control of asthma. Intramuscular glucocorticoids are risky and should be avoided.
6. UVA-UVB phototherapy (combination of UVA plus UVB and increasing the radiation dose each treatment, with a frequency of two to three times weekly). Narrow band UV (311 nm), PUVA photochemotherapy also effective.
7. In severe cases of adult AD and in normotensive healthy persons without renal disease cyclosporin treatment (starting dose 5 mg/kg per day) is indicated when all other treatments fail, but should be monitored closely. Treatment is limited to 3 to 6 months because of potential side effects, including hypertension and reduced renal function. Blood pressure should be checked weekly and chemistry panels biweekly. Nifedipine can be used for moderate increases in blood pressure.
8. Patients should learn and use stress management techniques.
9. A suggested algorithm of AD management is as follows:
Baseline therapy of dryness with emollients
Suppression of mild to moderate AD by prolonged topical pimecrolimus or tacrolimus and continued emollients
Supression of severe flares with topical glucocorticoids followed by pimecrolimus or tacrolimus and emollients
Oral and topical antibiotics to eliminate S. aureus
Hydroxyzine to suppress pruritus
Website: http://www.aad.org/pamphlets/ eczema.html.

Lichen Simplex Chronicus
Lichen simplex chronicus (LSC) is a special localized form of lichenification, occurring in circumscribed plaques; it results from repetitive rubbing and scratching. Lichenification is a characteristic feature of atopic dermatitis, whether generalized or localized. Lichen simplex can last for decades unless the rubbing and scratching are stopped by treatment. It occurs in individuals older than 20 years, is more frequent in women, and possibly more frequent in Asians.
Pathogenesis
A special predilection of the skin to respond to physical trauma by epidermal hyperplasia; skin becomes highly sensitive to touch. The very abnormal itching hyperexcitability of lichenified skin arises in response to minimal external stimuli that would not elicit an itch response in normal skin. Emotional stress in some cases. It becomes a habit and may persist for months to years, with resulting marked lichenification.
Skin symptoms mainly consist of pruritus, often in paroxysms. The lichenified skin is like an erogenous zone—it becomes a pleasure (orgiastic) to scratch. Often the areas on the feet are rubbed at night with the heel and the toes. The rubbing becomes automatic and reflexive and an unconscious habit. Most patients with LSC give a history of itch attacks starting from minor stimuli: putting on clothes, removing ointments, clothes rubbing the skin; in bed, the skin becomes warmer and the warmth precipitates itching. Many patients have AD or an atopic background.
Physical Examination
Skin Lesions
A solid plaque of lichenification, arising from the confluence of small papules; scaling is minimal except on lower extremities (Fig. 2-18). Lichenified skin is palpably thickened; skin markings (barely visible in normal skin) are accentuated and can be seen readily. Excoriations are often present. Usually dull red, later brown or black hyperpigmentation, especially in skin phototypes IV, V, and VI. Round, oval, linear (following path of scratching). Usually sharply defined. Isolated single lesion or several randomly scattered plaques. Nuchal area (female) (Fig. 2-18), scalp, ankles, lower legs, upper thighs, exterior forearms, vulva, pubis, anal area, scrotum, and groin.

In black skin, lichenification may assume a special type of pattern–there is not a solid plaque, but the lichenification consists instead of a multitude of small (2- to 3-mm) closely set papules—i.e., a "follicular" pattern (as in Fig. 2-14).
Differential Diagnosis
Includes a chronic pruritic plaque of psoriasis vulgaris, early stages of mycosis fungoides, ICD, ACD, epidermal dermatophytosis.
Laboratory Examination
Dermatopathology
Hyperplasia of all components of epidermis: hyperkeratosis, acanthosis, and elongated and broad rete ridges. Spongiosis is infrequent. In the dermis there is a chronic inflammatory infiltrate.
Management
Difficult. Repeatedly explain to the patient that the rubbing and scratching must be stopped. It is important to apply occlusive bandages at night to prevent rubbing. Topical glucocorticoid preparations or tar preparations such as combinations of 5% crude coal tar in zinc oxide paste plus class II glucocorticoids all covered by occlusive cloth dry dressings are effective for body areas where this approach is feasible (e.g., legs, arms). Occlusive dressings: glucocorticoid preparations are usually applied first, followed by an occlusive (plastic) dressing (like saran wrap). Glucocorticoids incorporated in adhesive plastic tape are very effective and can be left on for 24 h. Unna Boot: a gauze roll dressing impregnated with zinc oxide paste is wrapped around a large lichenified area such as the calf. The dressing can be left on for up to 1 week.
Intralesional triamcinolone is often highly effective in smaller lesions (3 mg/mL; higher concentrations may cause atrophy). Oral hydroxyzine, 25 to 50 g at night, may be helpful.
Prurigo Nodularis (PN)

Is often associated with AD or occurs without AD. PN patients with AD are younger and have reactivity to environmental allergens, nonatopic PN patients are older and lack hypersensitivities to environmental allergens. As in LSC the underlying stimulus is pruritus. Dome-shaped nodules — several millimeters to 2 cm — develop on sites in which persistent itching and scratching occur (Fig. 2-19). They are often eroded, excoriated, and sometimes even ulcerated as patients dig into them with their nails. Usually multiple on the extremities. PN usually occurs in younger or middle-age females, who often exhibit signs of neurotic stigmatization. PN starts with piercing pruritus that leads to picking and scratching. Lesions persist for months after the trauma has been discontinued.
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Dyshidrotic Eczematous Dermatitis

Dyshidrotic eczema is a special vesicular type of hand and foot dermatitis. It is an acute, chronic, or recurrent dermatosis of the fingers, palms, and soles, characterized by a sudden onset of many deep-seated pruritic, clear "tapioca-like" vesicles; later, scaling fissures and lichenification occur.
Synonyms: Pompholyx, vesicular palmar eczema.
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Laboratory Examinations
Bacterial Culture
Rule out S. aureus infection.
KOH Preparation
Rule out epidermal dermatophytosis.
Dermatopathology
Eczematous inflammation (spongiosis and intraepidermal edema) with intraepidermal vesicles.
Course and Prognosis
Recurrent attacks are the rule. Spontaneous remissions in 2 to 3 weeks. Interval between attacks is weeks to months. Secondary infection may complicate the course: pustules, crusts, cellulitis, lymphangitis, and painful lymphadenopathy. Disabling because of severe, frequently recurring outbreaks.
Management
Wetdressing
For vesicular stage: Burow's wet dressings. Large bullae drained with a puncture but not unroofed.
Fissures
Topical application of flexible collodion.
Glucocorticoids
Topical
High-potency glucocorticoids with plastic occlusive dressings for 1 to 2 weeks.
Intralesional Injection
Triamcinolone, 3 mg/mL. Very effective for small areas of involvement.
Systemic
In severe cases, a short, tapered course of prednisone can be given: 70 mg/d, tapering by 10 or 5 mg/d over 7 or 14 days.
Systemic Antibiotic
For suspected (localized pain) or documented secondarily infected lesions (usually S. aureus; less commonly group A streptococcus).
PUVA
(See Generalized Psoriasis) Oral or topical as "soaks." Successful in many patients if given over prolonged periods of time and worth trying, especially in severe cases.

Dyshidrotic Eczematous Dermatitis

Nummular Eczema
Nummular eczema is a chronic, pruritic, inflammatory dermatitis occurring in the form of coin-shaped plaques composed of grouped small papules and vesicles on an erythematous base, especially common on the lower legs of older males during winter months; often seen in atopic individuals.
Synonym: Discoid eczema, microbial eczema.
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Epidemiology
Two peaks in incidence: young adulthood and old age. Fall and winter.
Pathogenesis
Unknown. Unrelated to atopic diathesis; IgE levels normal. Incidence peaks in winter, when xerosis is maximal. S. aureus often present.
History
Skin Symptoms
Pruritus, often intense.
Physical Examination
Skin Lesions
Closely grouped, small vesicles and papules that coalesce into plaques (Fig. 2-21A), often more than 4 to 5 cm in diameter, with an erythematous base with distinct borders. Plaques may become exudative and crust (Fig. 2-21B). Excoriations secondary to scratching. Dry scaly plaques that may be lichenified. Round or coin-shaped (Fig. 2-21A) hence the adjective nummular (Latin: nummularis, "like a coin"). Margins often more pronounced than center.
Distribution
Regional clusters of lesions (e.g., on legs or trunk) or generalized, scattered. Lower legs (older men), trunk, hands and fingers (younger females).
Differential Diagnosis
Scaling Plaques
Epidermal dermatophytosis, ICD or ACD, psoriasis, early stages of mycosis fungoides, impetigo, familial pemphigus.
Laboratory Examinations
Bacterial Culture
Rule out S. aureus infection.
Dermatopathology
Subacute inflammation with acanthosis and spongiosis.
Course and Prognosis
Chronic. Lesions last from weeks to months. Often difficult to control even with potent topical glucocorticoid preparations.
Management
Skin Hydration
"Moisturize" involved skin after bath or shower with hydrated petrolatum or other moisturizing cream.
Glucocorticoids
Topical Preparations
Classes I and II applied bid until lesions have resolved. Steroid impregnated tape. Intralesional triamcinolone, 3 mg/mL.
Crude Coal Tar
2 to 5% crude coal tar ointment daily. May be combined with glucocorticoid preparation. Tar baths are useful in patients with refractory lesions.
Systemic Therapy
Systemic antibiotics if S. aureus is present.
PUVA or UVB 311-nm Therapy
Very effective.

Autosensitization Dermatitis
This term refers to an often unrecognized generalized pruritic dermatitis directly related to a primary dermatitis elsewhere. For example, a patient with venous stasis dermatitis on the lower legs may develop pruritic, symmetric, scattered, erythematous, maculopapular, or papulovesicular lesions on the trunk, forearms, thighs, or legs, which persist and spread until the basic underlying primary dermatitis is controlled. Similarly, autosensitization may occur as an "id" reaction in inflammatory tinea pedis and manifests as a dyshidrosiform, vesicular eruption on the feet and hands (Fig. 2-22) and papulovesicular eczematoid lesions on the trunk.
The phenomenon results from the release of cytokines in the primary dermatitis, as a result of sensitization. These cytokines circulate in the blood and heighten the sensitivity of the distant skin areas. The diagnosis of autosensitization dermatitis is often post hoc, i.e., the distant eruption disappears when the primary dermatitis is controlled. Oral glucocorticoids hasten the disappearance of the lesions.

Seborrheic Dermatitis
Seborrheic dermatitis (SD) is a very common chronic dermatosis characterized by redness and scaling and occurring in regions where the sebaceous glands are most active, such as the face and scalp, the presternal area, and in the body folds. Mild scalp SD causes flaking, i.e., dandruff. Generalized SD, failure to thrive, and diarrhea in an infant should bring to mind Leiner's disease with a variety of immunodeficiency disorders.
Synonyms: "Cradle cap" (infants), pityriasis sicca (dandruff).
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Epidemiology and Etiology
Age of Onset
Infancy (within the first months), puberty, most between 20 and 50 years or older.
Sex
More common in males.
Incidence
2 to 5% of the population.
Predisposing and Exacerbating Factors
In immunocompetent patients there is often a hereditary diathesis, the so-called seborrheic state, with marked seborrhea and marginal blepharitis. May be associated with psoriasis as a pre-psoriasis state in which the patient later develops psoriasis; in some patients a mix of lesions (superficial scales on the scalp and eyebrows and polycyclic scaling patches on the trunk) suggests the use of the term seborrhiasis. There is reputedly an increased incidence in Parkinson's disease and facial paralysis. Also, some neuroleptic drugs are possibly a factor, but the disease is so common that this has not been proved. Emotional stress is a putative factor in flares. HIV-infected individuals have an increased incidence, and severe intractable SD should be a clue to the existence of HIV disease.
Pathogenesis
Malassezia furfur is said to play a role in the pathogenesis, and the response to topical ketoconazole and selenium sulfide is some indication that this yeast may be pathogenic; also the frequency of SD in immunosuppressed patients (HIV, cardiac transplants). SD-like lesions are seen in nutritional deficiencies such as zinc deficiency (as a result of IV alimentation) and experimental niacin deficiency and in Parkinson's disease (including drug-induced). SD develops in experimental pyridoxine deficiency in humans.
History
Duration of Lesions
Gradual onset.
Seasonal Variations
Some patients are worse in winter in a dry, indoor environment. Sunlight exposure causes SD to flare in a few patients and promotes improvement of the condition in others.
Skin Symptoms
Pruritus is variable, often increased by perspiration.
Physical Examination
Skin Lesions
Orange-red or gray-white skin, often with "greasy" or white dry scaling macules and papules of varying size (5 to 20 mm) (Fig. 2-23), rather sharply marginated (Fig. 2-24). Sticky crusts and fissures are common in the folds behind the external ear. On the scalp there is mostly marked scaling ("dandruff"). Scattered, discrete on the face and trunk. Nummular, polycyclic, and even annular on the trunk; diffuse involvement of scalp.
Distribution and Major Types of Lesions (Based on Localization and Age)
Hairy Areas of Head
Scalp, Eyebrows, Eyelashes (Blepharitis), Beard (Follicular Orifices); Cradle Cap (Fig. 2-23).
Face
The flush ("butterfly") areas, on forehead ("corona seborrhoica"), nasolabial folds, eyebrows, glabella (Fig. 2-24). Ears: retroauricular, meatus.
Trunk
Simulating lesions of pityriasis rosea or pityriasis versicolor; yellowish-brown patches over the sternum common.
Body Folds
Axillae, groins, anogenital area, submammary areas, umbilicus—presents as a diffuse, exudative, sharply marginated, brightly erythematous eruption; erosions and fissures common.
Genitalia
Often with yellow crusts and psoriasiform lesions.
Diagnosis/Differential Diagnosis
Usually made on clinical criteria.
Red Scaly Plaques
Common
Mild psoriasis vulgaris (the two diseases can sometimes be indistinguishable), impetigo (rule out by smears for bacteria), dermatophytosis (tinea capitis, tinea facialis, tinea corporis), pityriasis versicolor, intertriginous candidiasis (KOH: rule out dermatophytes and yeasts), subacute lupus erythematosus, "seborrheic" papules in secondary syphilis (darkfield: rule out Treponema pallidum).
Rare
Langerhans cell histiocytosis (occurs in infants, often associated with purpura), acrodermatitis enteropathica, zinc deficiency, pemphigus foliaceus, glucagonoma syndrome.
Laboratory Studies
Dermatopathology
Focal parakeratosis, with few neutrophils, moderate acanthosis, spongiosis (intercellular edema), nonspecific inflammation of the dermis. The most characteristic feature is neutrophils at the tips of the dilated follicular openings, which appear as crusts/scales.
Course and Prognosis
SD is very common, affecting the majority of individuals at some time during life. The condition improves in the summer and flares in the fall. Recurrences and remissions, especially on the scalp, may be associated with alopecia in severe cases. Infantile and adolescent SD disappears with age. Seborrheic erythroderma may occur. Seborrheic erythroderma with diarrhea and failure to thrive (Leiner's disease) is associated with a variety of immunodeficiency disorders including defective yeast opsonization, C3 deficiency, severe combined immunodeficiency, hypogammaglobulinemia, and hyperimmunoglobulinemia.
Management
This chronic disorder requires initial therapy followed by chronic maintenance therapy. Topical glucocorticoid preparations are effective but can cause atrophy and erythema and telangiectasia, especially on the face, or initiation/exacerbation of perioral dermatitis or rosacea. UV radiation is beneficial for many individuals.
Initial Topical Therapy
Scalp
Adults
Effective over-the-counter (OTC) shampoos containing selenium sulfide, zinc pyrithione, are helpful. By prescription (U.S.), 2% ketoconazole shampoo, used initially to treat and subsequently to control the symptoms; lather can be used on face and chest during shower. Tar shampoos (OTC) are equally effective in many patients.
Low-potency glucocorticoid solution, lotion, or gels following a medicated shampoo (ketoconazole or tar) for more severe cases. Pimecrolimus, 1% cream, is beneficial.
Infants
For cradle cap, removal of crusts with warm olive oil compresses, followed by baby shampoo, 2% ketoconazole shampoo, and application of 1 to 2.5% hydrocortisone cream, 2% ketoconazole cream, 1% pimecrolimus cream.
Face and Trunk
Ketoconazole shampoo, 2%. Glucocorticoid cream and lotions: initially 1 or 2.5% hydrocortisone cream, 2% ketoconazole cream, 1% pimecrolimus cream, 0.03 or 0.1 tacrolimus ointment.
More potent glucocorticoid lotions (e.g., clobetasol propionate) may be used for initial control and are used along with the medicated shampoos.
Eyelids
Gentle removal of the crusts in the morning with a cotton ball dipped in diluted baby shampoo. Apply 10% sodium sulfacetamide in a suspension containing 0.2% prednisolone and 0.12% phenylephrine (use cautiously because it contains glucocorticoids). Sodium sulfacetamide ointment alone is also effective, as is 2% ketoconazole cream, 1% pimecrolimus cream, or 0.03% tacrolimus ointment.
Intertriginous Areas
Ketoconazole, 2%; if uncontrolled with these treatments, Castellani's paint for dermatitis of the body folds is often very effective, but staining is a problem. Pimecrolimus cream, 1%; tacrolimus ointment, 0.03%.
Systemic Therapy
In severe cases, 13-cis retinoic acid orally, 1 mg/kg, is highly effective. Contraception should be used in females of child-bearing age.
Maintenance Therapy
Ketoconazole 2% shampoo; tar shampoos may be equally effective; ketoconazole cream. If these do not work, then the old "standard," 3% sulfur precipitate and 2% salicylic acid in an oil-in-water base is effective; this must be properly compounded. Also, 1 to 2.5% hydrocortisone cream qd will work, but patients should be monitored for signs of atrophy. 1% pimecrolimus cream and 0.03% tacrolimus ointment are effective.

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Asteatotic Dermatitis
Synonym: Eczema craquelé (French craquelé, "marred with cracks," such as in old china and ceramic tile).
A common pruritic dermatitis that occurs especially in older persons, in the winter in temperate climates—related to the low humidity of heated houses. The sites of predilection are the legs (Fig. 2-25), arms, and hands but also the trunk. The eruption is characterized by dry, "cracked," superficially fissured skin with slight scaling. The incessant pruritus can lead to lichenification, which can even persist when the environmental conditions have been corrected. The disorder results from too frequent bathing in hot soapy baths or showers and/or in older persons living in rooms with a high environmental temperature and low relative humidity. The disorder is managed by avoiding overbathing with soap, especially tub baths, and increasing the ambient humidity to >50%, by using room humidifiers; also using tepid water baths containing bath oils for hydration, followed by immediate liberal application of emollient ointments, such as hydrated petolatum. If skin is inflamed, use medium-potency glucocorticoid ointments, applied twice daily until the eczematous component has resolved .

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